Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load.

中文翻译：

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Lamellipodial肌动蛋白网络的负荷适应。

对抗膜聚合的肌动蛋白丝增强了内吞作用，囊泡运输和细胞运动。体外重建研究表明肌动蛋白网络的结构和动力学对机械力有反应。我们证明膜细胞张力调节时，迁移细胞的lamellipodial肌动蛋白响应机械负荷。在稳定状态下，迁移的细胞细丝采用Arp2 / 3产生的70°分支点定义的规范树突状几何形状。张力的增加触发了角度范围扩大的致密网络，而张力减小则导致向稀疏构型的转变，该构型主要由垂直于质膜生长的细丝主导。我们显示出这些反应来自支化肌动蛋白的几何结构：当每根灯丝的负载减少时，伸长速度增加，垂直长丝逐渐超过其他长丝，因为它们聚合到膜的最短距离，从而保护它们不被覆盖。此网络固有的几何自适应机制可响应机械负载来调整突出力。